Physiological and Pharmacological Characteristics of Quisqualic Acid-Induced K+-Current Response in the Ganglion Cells of Aplysia.

Abstract

Glutamate is a major neurotransmitter for excitatory synaptic transmission in the central nervous system (CNS) of the vertebrate and the invertebrate. Besides producing the fast excitatory synaptic potentials in the CNS, the glutamatergic synapse plays an important role in the formation of synaptic plasticity, such as learning and memory. An excessive release of glutamate from the synaptic terminal is thought to be one cause for apoptosis, neuronal death. Glutamatergic synaptic transmission is also important for the understanding of various neuronal diseases.In glutamatergic synapse, fast excitatory postsynaptic potentials are produced by the activation of ionotropic glutamate receptors (iGluRs), which consist of receptor-cation channel complexes as revealed by cDNA cloning. The iGluRs have been subdivided into the NMDA-, AMPA-, and kainate-receptor subtypes by their pharmacological profiles [1]. Glutamate can also activate metabotropic glutamate receptors (mGluRs), which are coupled to G proteins and a subsequent intracellular messenger system, such as phosphatidyl inositol (PI) turnover. Usually an activation of the mGluRs produces slow synaptic potentials and primarily mediates the modulatory function of the cell Key words: quisqualic acid, glutamate receptor, molluscan neuron, potassium channel. Abstract:The extracellular application of either quisqualic acid (QA) or Phe-Met-Arg-Phe-NH 2 (FMRFamide) induces an outward current in identified neurons of Aplysia ganglion under voltage clamp. The time course of the QA-induced response is significantly slower than that induced by FMRFamide. The reversal potential for both responses was Ϫ92 mV and was shifted 17 mV in a positive direction for a twofold increase in the extracellular K ϩ concentration. The QA-induced response was markedly depressed in the presence of Ba (A)-channel blocker, had no effect on the response. The QA-induced K ϩ -current was significantly suppressed by CNQX and GYKI52466, antagonists of non-NMDA receptors. However, the application of either kainate or AMPA, agonists for non-NMDA receptors, produced no type of response in the same neurons. The QA-induced K ϩ -current response was not depressed at all by an intracellular injection of either guanosine 5Ј-O-(2-thiodiphosphate) (GDP-␤S) or guanosine 5Ј-O-(3-thiotriphosphate) (GTP-␥S), but the FMRFamide-induced response was markedly blocked by both GDP-␤S and GTP-␥S in the same cell. Furthermore, the QA-and FMRFamide-induced K ϩ -current responses were both decreased markedly when the temperature was lowered to 15°C, from 23°C. These results suggested that the QA-induced K ϩ -current response is produced by an activation of a novel type of QA-receptor and that this response is not produced by an activation of the G protein.

Evidence That the Swim Afferent Neurons ofTritonia diomedeaAre Glutamatergic

“…Identical DMSO-containing drug-free solutions were used to control for effects of the DMSO itself. Studies in various molluscs (Storozhuk and Castellucci, 1999, Kimura et al , 2001, Hochner et al , 2003, Lima et al , 2003, Piscopo et al , 2007) as well as hippocampus (Poncer et al , 1995, Du et al , 2000) have used CNQX in the concentrations employed in the present study (100 – 300 µM) to block glutamate responses.…”

Augmenting Effect of Serotonin on the Voltage-Dependent Ca2+ Current and Subsequently Activated K+ Current in Aplysia Neurons

“…The volume ratio described above is an underestimate because the surface tension of the droplet is larger in air than in water. Thus we used a correction factor of 1.5 as the volume ratio, which was determined by measuring sizes of the droplets ejected from the same electrode in the air and in paraffin oil (Kimura et al 2001).…”